B (2:18)

Sure, Moni, I'd love to. We are the internal medicine podcast. We Use expert interviews to bring you clinical pearls and practice Changing Knowledge Tonight we have a fantastic conversation with our guest, Dr. Pandra. He's a professor of medicine and the director of the Heart Failure and Mechanical Circulatory Support Program and Infiltrative Cardiomyopathy Program and the director of GW's heart and vascular Institute at the George Washington University School of Medicine and Health Sciences in Washington, dc. He is an advanced heart failure and transplant cardiologist. He has a keen interest in education, in developing educational programs nationally and internationally, and in developing innovative solutions and clinical program building to improve equitable heart failure care. He has served as co editor of Heart Failure self assessment programs on editorial boards including JAC Heart Failure and directed development of heart failure curriculum for PCPs in Latin America. He has spoken widely at both national and international meetings. Dr. Pandroth is governor for the Washington D.C. chapter, past chair of the Heart Failure and Transplantation Section of American College of Cardiology. And tonight we went through some really great tips for guideline directed medical therapy initiation and a lot of on the transitions of care during the hospitalization as well as a lot of key pearls for diuretic therapy to think about. So without further ado, let's get to it.

C (3:41)

A reminder that this and most episodes will be available for CME credit for all healthcare professionals through VCU Health at curbsiders vcuhealth.org okay Dr. Pandrath, welcome to Curbsiders. We're very excited to have you. We like to start by getting to know our guests a little bit past medicine. So can you start by telling us a little bit about a hobby or interest you have outside of medicine?

E (4:04)

First Glad to be here. So thanks for having me. And you know, in terms of outside medicine, I actually love traveling. That's one of the things I you know, anytime I can get on a plane, a flight or drive somewhere, that's one thing I do. Other thing is I love cooking. And cooking is not just a hobby, it's a passion. I actually in the process of writing a cookbook and even though I'm a heart failure card carrying heart failure transplant cardiologist, I also have been kind of involved a lot of food nutrition related projects over the last a couple of years. So yeah, I love to cook for myself obviously because I love to eat but for friends, family and you know, compile recipes and create recipes as well.

B (4:55)

Do you use salt in your recipes?

E (4:58)

Well, you know, do I have to give the official answer for that or the unofficial answer? But no, I actually, I mean I do very controlled salt, you know, bare minimum as needed. We do have a lot of salt in the diet as it is in all the different ingredients, so I try to control that.

C (5:18)

And what's your favorite cuisine to cook?

E (5:20)

Oh, boy, that's a tough question because I actually cook almost everything. But, you know, again, yeah, I don't. I wouldn't draw favorites. Asian is more kind of close to home food. And Asian would be across the board. Not only Southeast Asian, the subcontinent, but even across Thai as well as Malaysian food. But, you know, as I said, even French, Italian, everything.

B (5:47)

So in your travels, is there somewhere you've specifically enjoyed going for the food?

E (5:52)

That's actually a great question. I spent summer in France, actually driving through Burgundy and the Champagne area, and it was this amazing food, but, you know, really fresh ingredients. You didn't really even need to add much. But, you know, Vietnam is actually, I would say, one of the places where I love going for food, and I've been there twice, and I just. Amazing food. It's healthy. It's so many different vegetarian options. I do eat meat as well, different kinds of protein, but it's just fabulous, the food out there.

B (6:32)

Awesome. So we'll switch gears and I guess ask one more question. What is some meaningful advice or feedback that you've received throughout your career?

E (6:43)

There's a lot of advice. I've been fortunate to work with some remarkable people. And early on, I think during my early days of postdoc years as a clinical researcher, I had a mentor who I always finally look back on, and he was. One of the advice he always gave me from a kind of academic perspective was, you know, don't write papers. Just to write papers, you know, it's really important. Write something which is meaningful. Now, quantity doesn't matter. Quality matters. And I actually do kind of keep that to heart. And, you know, as you go through different parts of your training, your phases of life, and the other thing which you know is your own well being. And I know, well, being is a big word right now, but it's not in just kind of as a. As a buzzword, but it really means something. You really have to take care of yourself. Whether. And well, being can be in different ways. And it's not only burnout at work, it's also, you know, being physically fit, taking care of your health, your nutrition, and doing things which you enjoy. And that's kind of what I, you know, have been given the advice.

B (7:52)

I definitely think the first one is near and dear to Moni and me right now. So appreciate that advice for us. On a personal level.

C (8:00)

I don't know.

B (8:01)

What you're talking about, but we'll leave it like that. Do you want to ask anything else or do you want to do picks of the week?

C (8:07)

Let's do picks of the week. Okay, so mine's pretty obvious. Not having Covid shout out to Binax for proving that I'm negative. Like, I don't know. I. You guys may not know this, but Meredith and I actually record in the same space, which is somewhat unique, I think, for the curb. And so the amount of contingency plans I had in my mind for if I did not convert to negative, really mind blowing. So anyway, so my pick of the week is the Binax.

B (8:37)

I mean, five years, maybe Binax has been the pick of the week in the background. Mine is also. It's September when we're recording this, so it's now football season and Moni and I had to actually go a full day without speaking to each other because her Michigan Wolverines were playing my Texas Longhorns and Texas won. And I did confer with Moni afterwards that we could still be friends. So it'll be okay. But it was a glorious day.

E (9:08)

That's amazing.

C (9:09)

That was uncalled for, but definitely I should have seen that coming. So anyway, so Meredith, that's fantastic. I'm happy for you, really, because we just won the national championship. Please take us to Cash back for our first case.

B (9:25)

So we will start with Ms. Anita Breath, a 64 year old female who presented to the emergency room with shortness of breath, bilateral lower extremity swelling and fatigue. Over the past week, she's had a long standing history of poorly controlled type 2 diabetes, hypertension and tobacco use. She has noticed a gradual increase in shortness of breath that initially only occurred with exertion. Most recently, however, she's noticed she's not been able to lay flat and her shortness of breath has been worsening at rest. During this time, her feet and legs have become more swollen. At home, Ms. Breath takes Metformin 1000 milligrams twice a day, Lisinopril 20 milligrams every day, and Metoprolol 25 milligrams twice a day. In the ER, her oxygen saturation is 91% on room air, blood pressure is 155 over 90 and a heart rate of 93. On physical exam, there's jugular venous dissension and an S3 gallop. The bilateral lower extremities are cool to touch and there's three plus pitting edema to her thighs. A chest X ray obtained in the emergency room shows vascular congestion and her BNP is 1,100. The troponin, serum, creatinine, electrolytes are all normal. And an EKG demonstrates normal sinus rhythm with few PVCs. So I think where we kind of wanted to start was does this seem like a typical patient presentation for acute decompensated heart failure and what other history and maybe physical exam findings you may want to know?

E (10:51)

Well, you know, that's a, that's a great presentation, which we, you know, is a very common presentation, I would say. And you know, just going back, actually reflecting on what you said earlier, that I'm following up on yours right after Michelle Kitterson and I just admire and I had the honor of co chairing with her a recent update on hfp. And this is something, I'm sure she talked about it as well. So initially, I think when we get somebody like this, I know we're talking about heart failure here, but really you have to go back to the basics. You have to make sure, is this really heart failure? That's the first thing. And because everything which is somebody is short of breath or has leg swelling, you really have to go through those differentials. What we have learned over the years of training through medical school as well as residency training, because there's so many other causes in somebody with comorbidities that this could be a mimicker for heart failure. Not having known what the LV structure and function is, I think the clinical presentation becomes important. So starting from the point one, you know, obviously history, the, you know, what are the risk factors that person could have. And in this particular case, you clearly have fully controlled hypertension. She's presenting very hypertensive, she has leg edema, she has SV gallop, she has, you know, every sign or symptom suggestive of acute heart failure. Now, this is where you would start off with applying all the knowledge you have from what the definition of heart failure is. And this is where you will apply the universal definition of heart failure. I'm sure you talked about it in the past. This is the definition which was proposed by Heart Failure Society and now has been adopted by all the guideline for heart failure from ACCHA guidelines as well. And you incorporate your signs and symptoms of heart failure, suggestive heart failure, and then you go and look at the biomarkers. And so that's something beyond history, beyond those risk factors, beyond the acuity and the chronicity of the symptoms. This is what you want to know. And that's going to help us decide if this is something else. Now, you also want to know if there's anything suggestive of liver disease or any other, you know, any other markers of other systemic illnesses, such as thyroid, are they having an arrhythmia? Anything which either could be an etiology towards heart failure or could be overlapping with a presentation of heart failure.

B (13:30)

And I think just where we are also in the course of medicine right now. I was curious too. When she's presenting, do you see much role for like, point of care ultrasound as being helpful?

E (13:42)

Yeah, I mean, that's, you know, the point of care ultrasound. The role for it has been emerging quite a bit over the years now and from multiple levels. You know, a lot of times we kind of persuade on the LV ejection fraction. But the point of care ultrasound can do much more than that. So this is somebody who's presenting, you know, with hypertensive disease. But you'll get an idea. If you use a point of care ultrasound, obviously you'll know the structure. A quick, you know, look at the structure of the heart. Is there left ventricular hypertrophy? But more importantly, you can also look at their vena cava. You can look at. Is that vena cava distended? Is there intravascular congestion there? So that kind of adds on to your level of suspicion or whether this is going to be acute heart failure and is the person really congestive or is there anything else which could be mimicking or presenting as low extremity sweating? Now, in this particular case, obviously she's hypertensive. Her heart rate is still high. But if this was somewhere you were also concerned about pericardial fluid around or effusions or tamponade or anything like that, that ultrasound would be helpful too. Now, there was a, you know, suggestion of any kind of acute ischemic injury that would be useful to look at wall motion, original wall motion. I would male at these tools.

B (15:00)

So would you say it would like in your practice does that point of care ultrasound? It's mostly there, it sounds like, to help, like, emphasize what you're already thinking versus really helping to like, decide one way or the other. Is that right?

E (15:15)

So, no. So I think what I really meant by saying that is it's an additive information. It can be so in this particular presentation because it, you know, what you just described, the. The patient is very hypertensive, has S3 gallop. So you're already kind of very have you have findings, clinical findings, both symptoms as well as clinical features, physical kind of findings which are very suggestive of heart failure. But if there was a little bit of ambiguity in there and there were other if there was somebody had Nash or had kind of marbur, obesity and, and with the diabetes, they also had, you know, liver involvement or had, you know, they were more sedentary and had concern about DVTS or pe. And then the RV failure aspect comes in. Or, you know, with all those different comorbidities, you could have pulmonary hypertension could be Group 2 pulmonary hypertension could be, you know. So any of those differentials will start coming in. Yes, the final cascaded heart failure. But that would help you kind of decide if this was heart failure or non heart failure. But in this particular presentation, yes, it's more to confirm.

B (16:29)

Got it.

A (16:33)

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D (18:09)

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C (19:27)

Yeah, I think in this particular patient, if I recall, doesn't actually have a known diagnosis of heart failure. So I think there's a two pronged question. So in this situation where the patient doesn't already have a diagnosis of heart failure, when is the right time to get an echo? And then the other side of that is when or should we get an echo for a patient that comes in and has a heart failure exacerbation but already has a known diagnosis of it? So let's start with the not known part and then we'll go from there.

E (19:57)

Yeah, that's actually, you know, this is something which is addressed in the guidelines as well as the expert consensus documents. Now, you know, when somebody comes in, has no known diagnosis, they definitely need some assessment because it's going to tell you a couple of things. It's going to tell you structure of the ventricle of the atrium. So it's going to, it will help you go down your differential of is this really heart failure? Now I'm assuming that you already have your biomarker levels, your anti pro, BNP or bnp, whichever is available in your practice or in the hospital setting. And that's already given you a second level of confirmation of your or meet whether you meet the criteria for the universal definition of heart failure. So now the echo is really helping you pinpoint and decide what kind of therapy are you going to use? Are you going to go for HFREP therapy, HFpEF therapy? And now in these days, a lot of its overlap is there's a big overlap. Almost, you know, out of the different medication classes, you pretty much use almost all of them in both sides, depending, with some nuances, depending on the ejection fraction and some other criteria. But then it also tells you the anatomical features of what could be causing that heart failure. So as we, you know, as you look at hypertrophic ventricles or enlarged atria, that's going to guide you to a different differential within heart failure itself. So I, based on my own practice and as well as the guidelines, as well as the expert consensus documents, it's recommended you should get an echocardiogram of anybody with a suspicion for heart failure. So now going back to your second question, Moni, which was, you know, somebody already has a diagnosis of heart failure and they're coming in for exacerbation. Now, whatever the etiology may be, maybe, you know, they have arrhythmia, they may have infection, may have thyroid disease, they have, you know, you name it, but it could be. But that is a different situation. You really don't need to just repeat routine echocardiograms unless you have a question which is going to be answered and is going to change your management. Now if somebody is coming in and they are, let's assume they are congested and right now it's not a concern about low output failure, they're just congested, they're in your, if you look at your classic hemodynamic classification, they're in the quadrant of wet and warm, they have a blood pressure, they are warm, they just congested, they have all the signs of increased bleeding pressure. In this person, your treatment is going to be decongestive therapies. That's going to be the main goal initially to relieve the symptoms. So getting an echo is not going to be additive in the sense that you're not going to really change your management. Now at some course, if that situation changes in the sense that they are not responsive to your initial treatments or there's a clinical decompensation, they become hypotensive or you are worried about something else going on and then getting an echo would be a good thing. Same thing is for, you know, if you are treating somebody and you had an echo and is there any usefulness of repeating an echo? And that again should be driven out of the question. What am I going to do with this knowledge? What I'm going to obtain from echocardiogram to change my treatment? If it's just like, oh yeah, I'm just already have the information I'm going to treat it and I'm going to send them out. That's different. But now, if somebody had a lot of valvular regurgitation, somebody had moderate to severe valvular insufficiency, whether it be mitral valve, tricuspid valve, and you say this is a volume dependent state and I want to reassess it after I decongest them, I want to know what's the severity of that valvular insufficiency. Am I going to really address this in this particular hospital, say, because now there's so many therapies out there for that or emerging therapies out there. So am I really truly assessing the severity of it? And that's when the repeat echo may be useful after you initiate the therapies?

C (24:12)

No, that's helpful because I think for a long time I had this practice pattern and this is a conversation I have with residents a lot where like they come in volume overloaded and they're like, well, they haven't had one in a while. Well, maybe we need to talk to the patient a little more and get a little more history about why it is that they might have had this exacerbation. Right. And the thing that I never put together until preparing for this and then also putting together things we do for no reason talk is I don't think I'd ever put together that like you can get like volume status dependent valvular changes. Right. And so I don't know why I didn't put that together, but I didn't. And very helpful to realize that because you don't want to go chasing something when it's like, well, this is something that actually might go away if you just give them the therapy that they require at that time.

E (24:59)

Yeah, we do see that a lot. I think, you know, when we initially get called on consults or just be primary and the level of valid insufficiency remarkably can go down with appropriate decongestion and other, you know, application of therapy. So really helpful getting that information.

B (25:20)

So I think talking a little bit about decongestion, that's actually a good segue for us. So for Ms. Breath, who's clearly like volume overloaded, we want to start a diuretic like therapy for her. For her. She's obviously going to be like naive to that therapy, but wanted to kind of get a little bit of your insight on how we would start her diuretics.

E (25:42)

Yeah, Meredith, that's a great question. And you know, something which we all deal on a daily basis. Right. So I think she's diuretic naive. So that's a good thing. Knowing what her starting electrolytes are, especially kidney function is helpful, especially because as you try to gauge what kind of dosing you're gonna do. So, you know, obviously the guidelines recommend that, and most of us have a practice of saying if you are naive, you can just start with furosemide, for example, and usually a 40 milligram IV dose. But I just want to make a point on this particular presentation because in her case, she's also hypertensive. So while you are going to decongest her, a lot of it's also going to be after the reduction, and that is key. Sometimes they miss that point. As we focus on the decongestive part of therapy in patients with hypertensive heart failure, we are not aggressive enough on the hypertensive, especially the afterload reduction. So that has to be going hand in hand because otherwise people, or you, like all of us, will get into trouble pretty quickly in the sense that we'll keep trying to get that decongestion done and they're hypertensive and you start having kind of renal injury as well. So this is where I think it has to go hand in hand. And this goes back to those basic four quadrants of kind of, you know, hemodynamic principles and physiology, because as you reduce afterload, you're going to have a better kind of overall output, better diuretic effect, and it's going to augment you. So that's number one. Now, going back to the choice of diuretics and the dosing, you know, it's just Covid. You know, if they're totally naive, they're kind of depending on what kind of how much volume overload they have, you could, you know, somebody's older, somebody is not, you know, it's mildly overloaded. And mild is such a kind of subjective, vague term. And especially if somebody has a lot of kind of splanchnt congestion, you're not going to see that. But, you know, based on their symptoms, you could do a 20 or 40 of fierce mite as a bolus first and then see what their response is. And you can gauge the response in two hours and see what the. How they're responding to it. If they're responding well, then you can then decide on your next dose. You can stick with the bolus. Now, if they are not responding and you gave another bolus, or you increase the dose from either 40 or 80 furosemide, or they were already so volume ollated, they ended up getting 80 in the beginning. And depending on response, if they're not, then you want to increase either the dose or the frequency or sometimes both. And that becomes important because just giving the same dose over and again is not going to work because you're gonna have breaking phenomena, you're gonna have. You need to really reach the threshold.

B (28:23)

I wanna go back in a minute to the afterload part, cuz I think that's actually a good point. I wanna talk about. Um, but when you're thinking about increasing the diuretic and you're doing increase to frequency for bolus dosing still is there a maximum amount that you would do that frequency at for let's say furosemide?

E (28:43)

Yeah. No, you can go like three, four times a day. So you can go that. The question to ask is at that point is that strategy really working? And that's if you have to go so frequent, that means either you are not getting the amount of response you want or there's something else kind of interfering. Whether there's underlying kidney disease. There's either acute or chronic kidney disease and there's diuretic resistance even usually not in a naive patient. But you can have breaking phenomena. It also could be, is there anything else? I mean is there simple things like you know, is there any obstructive uropathy? Is, you know, is the bladder full? Are they even making the urine? Or is that obstruction in the bladder area so the bladder urinary retention. So those are kind of things I would first alongside look at. There are other tricks you can do. You can also always look, look at a spot urine sodium and you know, after a bolus you can check spot urine sodium in a few hours and see if you know they are appropriately responding to it or not. And so that's the trick. And actually that's in the guidelines and actually talking about guidelines, I do want to just kind of for the audience refer them to a latest document which came out this year on acute heart failure management, which is an update of a document from 2019. So I encourage your listeners to kind of take a look at it because it's a very practical advice. And this is not that a large guideline document with 1, a 1, 2 and 3s. And all of us know sometimes after two pages we jump to the last page and done. But this is bite size information, very succinct, very practical information. What to do in different settings, same thing like HFrEF, HFPEP and now with acute heart failure as well so, Meredith, going back to the question you mentioned about the dosing of the frequency, so the other strategy, which I personally use is a drip, an infusion. So if I see the patients are not responding, I go to the infusion, and I'm sure you're going to ask, come back and say, oh, well, that's great. What about the dose trial? Is that something coming, or am I taking your thunder away?

B (31:06)

Yeah, you take it. You know what I'm going to ask.

E (31:09)

Okay. So this is remarkable because if you think back, and the dose trial, which was a few years back now, was comparing bolus dosing versus continuous infusion, and, you know, it didn't show any difference in outcomes, but the outcomes were different. When you look at the total urine output, it's a little different outcome in decongestion rather than changing mortality. My goal at this point, I'm on the bedside. I'm the one taking care of. Or you're the one taking care of it. Right now, my goal is not what's going to happen 30 days or a month after in terms of mortality. Right now, the goal is, what's the urine output? Am I getting? And if you look at the dose trials, there were some issues with the inclusion criteria who were included in the population. So it's a little different. So that sometimes it doesn't apply to a lot of our clinical patients we see in practice, and we know that a chronic or a continuous infusion gives us a better result. So, yeah, that's my usually thing is, if somebody is not responsive, if I'm giving them boluses one after another, I'll move over to infusion. And that infusion can be, you know, you can go up to 20 milligrams per hour.

B (32:22)

Okay.

E (32:22)

Of furosemide.

B (32:24)

Yeah. So let's say you. You have someone who's not naive, so you would increase their furosemide dose, kind of max them out on dose, then increase frequency, and then go to a drip or.

E (32:35)

Yeah. So if I go to 80 IV and if they're not responding, that obviously you really need to go to a. Twice a day, thrice a day dosing. And then if they're not responding to that, you already know, if you have given somebody two doses and they have not responded the way they're supposed to respond, you already know. So there's no point waiting till another day or two days. You really need to move fast on those patients and say, okay, I'm going to switch over to a different strategy. And then the question is, if this was not A naive patient. This was somebody who was already exposed to loop diuretics, which would be the most commonly used ones. And that's the time when you start asking, why are they not responding? Is it because there's so much splanking congestion? Is it because they're not absorbing? Is it because the CKD or the chronic kidney disease? In that case, you can use also other agents such as bumatonide and torsemide. And obviously there have been trials around that, too. But we all agree, or I think a lot of people in the heart failure world will do that as they move over to a different loop diuretic. Now, if that doesn't work either, then you really need to start adding adjunct diuretics. And the adjunct diuretics really need to focus on some other aspect of the Nephron. So the way to remember is all these diuretics are working on some aspect of the Nephron, right? Some are working on the loop of Henleins, some are on the proximal tubule. So you really want to have another adjunct diuretic targeting another area. So adding two. So, like doing two loop diuretics is not going to give you the results. So add a thiazide on top, whether it be chlorthalidone or, you know, something else or, you know, a lot of people visit metalazone. And there have been studies on that as well. You know, without boring you with the names. They've been, you know, different, smaller studies looking at comparing clothalidone versus methalazone. And then there's also factors of cost which come in. Usually clothalidone IV tends to be more expensive.

B (34:42)

What are your thoughts then when you're getting to that point where you're thinking about adjunct diuretic therapy? What are your thoughts then on adding, like, say, an SGLT2?

E (34:53)

Great, great. This question would not have been there a few years back, right? So now we have this in our armatorium, and actually there is data now to support this in. So I can confidently say that as well as it's in your guidelines now to say early use of agility to inhibitors, because that will help you for in adjunct dialysis as well. In fact, this is very important because if there was somebody you initially are going to really, you know, scale up your diabetic therapy and you're starting AGLT 2, and as you start reassessing them on a daily basis of where they are, where the progress is, and you have to kind of take a pause and say, okay, they're responding appropriately, and they're coming down on their kind of volume state or filling pressures, then you may even have to back off on your dietic strategy because HGLT2 inhibitor is going to stay. And if they're not responding, obviously that's a different story. But SGLT2 early on is very beneficial now. And the good thing about it, it doesn't have a blood pressure lowering problem. So in patients, in this particular patient, which we talked earlier was hypertensive, but if this was say somebody who is href or heart failure with renewed ejection fraction and their blood pressure was low to begin with, and you really don't have many other choices and LGLT is remarkable.

B (36:23)

And then I think the other study that came out fairly recently was also like the added effects with acetazolamide, but that study came out kind of without SGLT2s. And so just like in your opinion, you would, I assume based on how the guidelines are written, you would favor the SGLT2 before you go to adding acetazolamide, even on the inpatient side.

E (36:46)

Oh, definitely. Because remember, HLT2 is multifold, right? The use is multifold because you have, you know, across the spectrum of heart failure, doesn't matter what ejection fraction. Now it has supportive evidence across the whole range, across the genders. So it's not gender specific. It's not. It has multiple benefits, chronic kidney disease, you know, in some even liver disease now. And there's a small data kind of emerging there, obviously, you know, diabetics and cardiovascular disease. So it's a disease modulating therapy which has the added benefit of being, providing that adjunct dialysis. So etazolamide is a pure diuretic, adjunct diuretic. So, you know, to choose between those two, there's. To me, it is no brainer. You go with SGLT2. Now on top of that, if you need something. Yeah, it is a little minor.

C (37:42)

Okay.

B (37:43)

And then I just wanted to go back to the afterload reduction part that you brought up at the beginning of this part of the conversation. So for her, I'm trying to like think about how I'm favoring those things. So I often, I like, would see her and I'm like, hey, she needs to be diurese. And so I'm favoring that. But it sounded like from the beginning that actually maybe some of the first meds I should be thinking about are her afterload reduction, even before diuretic therapy.

E (38:08)

So, you know, she's congested. So I think that you're right on the Money, you need to decongest. There's no questions about that. Right. So because you need to leave the symptoms now, that's one. Because it's the total overall volume state. So that's afterload is going to help alone. But in this particular case now if she was even more hypertensive, let's say she was like you know, 170s, 180s now because 150, you don't know is she hypertensive at this point because she, so she has respiratory distress or discomfort that she's totally volume overloaded and that's driving the hypertension. And as you relieve her that volume overload state, the blood pressure may come down or is this hypertension causing that kind of edema, flash edema as well as that. So you start off with the diuretic, you know what the blood pressure is if it's still high. And that's the time when you kind of start focusing on afterload. So the first thing is still going to be diuretic.

C (39:10)

I think all this is very helpful. Going through the diuretics. The thing that drives me bonkers and I think a lot of hospitals bonkers is the struggle for accurate ins and outs. So it's sometimes hard to kind of accurately know how someone's doing. So what are some kind of hacks that you have to approach that part of it because like you can't change their therapy if you don't know whether or not it's working.

E (39:36)

Yeah, that's again a million dollar question. And we can go from really a poor mind solution to really first world problems. Right. So I think we have a spectrum of options in our armatorium there simple thing, simple. Obviously unfortunately, which doesn't happen as frequently as we want. Accurate in and out for multitude of factors. But then on top of that body weight is useful. But remember, you just have to be a little bit of be careful on the body weight. So that's something which we have used for ages. That's the cheap way of doing it. You have a scale, nothing cheaper than that. Every hospital has one, every practice has one. You can put somebody on it, you can check it. Now the only thing to be careful is when you are looking body weight interpretation in the acute setting that's useful on a daily basis. The delta change is useful. But when you start looking at long term changes and somebody in the hospital for a long time and they're not eating, what about the nutrition or they're eating too well, they were not eating well before, you really have to start factoring those other factors as well, which sometimes we don't because we think assume that everything which is changing the weight is all fluid. But again, if going back to if you said the first day they came in diabetic and a couple of days you're assessing using body weight, that's a very useful marker, especially in and out. So those are too simple things. Now beyond that you can do is, you know, if somebody has a diagnosis and this is where if they are the appropriate candidates for pulmonary artery monitors, such as, you know, implantable pulmonary artery monitors in there, those can be useful because if they already have it, somebody who has especially high risk for readmission, a lot of practices would use that as well. And if you have that already in place, then you could actually assess it and see, evaluate and know what your pulmonary pressures are and get you an idea whether they are responding to it. There are some nuances in there because there's always a question about concordance and discordance in pressure and volume, but those are a little more rarer issues.

C (42:00)

Yeah, I think I actually had not heard about the pulmonary artery monitor as much. I don't know if that's newer than how old I am in training, but that's. That's an interesting one.

D (42:15)

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C (45:09)

One of the things, and I'm just going to kind of say it because it's something that I've done in the past. One of my interns when I was a med student actually taught me this, which is if the patient seems pretty reliable and they're like on top of it, it's like go in with a pen you don't mind losing and a sheet of paper and have them write down their eyes and nose. And a lot of times I've noticed patients get super like they're very excited to be able to contribute to their care. And so that's something I've used. It's very patient specific. But the ones that you do it on that it's worked for me, I don't know if you've tried that or.

B (45:41)

This is the first time you've ever said that, so. Or told me that story, which is mind blowing to me, but I've never done that. But I do similarly ask like I try to really assess from them when their urine output, like especially the transition from the ER where that urine output is usually not as well recorded sometimes. And so like I asked them how robust it was. So I'm like, were you filling these up quickly or not? And I use that sometimes especially to break ties.

E (46:10)

But and I also remember, depending on your practice and your population, if you have a lot of elderly patients, geriatric patients, a lot of incontinence, people have diapers, people have, you know, pads. So those factors come in because there's no way they're going to record that. So you know, you really unfortunately then you have to start like looking at how many pads that you kind of change and get a rough estimate of are they responding or not. And as I said, you can also use, I mean beyond the bedside, which are obviously the easiest things to do. Then you can also look at like urine, sodium. Are they responding? That's another measure. Yeah.

C (46:53)

And kind of the last little elephant in the room. And I think we've talked about this on one of our things we do for no reason episodes but the sodium and fluid restriction in the hospital, I think there's something about the RAS activation system like this may not be the best idea. So I was just curious your thoughts on that.

E (47:09)

Yeah. So you know that science around sodium and fluid has been kind of going back and forth, back and forth. I mean, I think as in general, as Americans, we all have a very high sodium diet to begin with. So I think level of restriction in the sodium is a good thing, you know, to the fine level of what that does to wrath activation in the acute setting. There's also is the same kind of principles around. Bolus dosing was also there. Bolus dosing of diuretic versus continuous. So it doesn't really fully pan out scientifically 100% because if you look at the data and you have two camps on that. But I do think if somebody's totally volume overloaded, it's reasonable that there's a level. I mean if they're drinking gallons, which that's a different story. But most of the people I feel are not drinking gallons of fluid when they already show short of bread. Sodium is a different problem because sodium, unfortunately, just because of what everybody in a world where food Insecurity is so prevalent and that's what you can get your hands on is usually high sodium diet. And so yeah, controlling sodium, but on the other hand making it so bland that they don't want to eat anymore. And the time and nutrition is important, especially in patients who are elderly who also need a little oncotic pressure. They need that albumin and now they're not going to eat anything because the food is like this. So I think, you know, just common sense making sure that they're not, they don't have a bag of chips and lays around or you know, a nice salty burger around in the bedside. But I don't think starvation is the right thing either. But as the guidelines recommend 2 grams of sodium a day and you know, we, in my practice, I, if I am, I think a patient reliable and depending on the degree of volume or load, I may say, you know, between 48 ounces to 64 ounces of fluid.

B (49:07)

So I guess we'll go ahead and move on with the case a little bit. So Missed Breath is admitted to the hospital. Obviously we've been talking about that. And she begins receiving her IV furosemide. And her echo reveals that her EF is 30% with signs of left ventricular hypertrophy and mild to moderate mitral regurgitation. So given both her original symptoms as well as this new echo we got for her to diagnose her, how would you classify her heart failure?

E (49:40)

So you know, obviously she has a heart failure based on the clinical symptoms. So I think this is something important. As you talk to the patient and you know, you're the front line, you're talking to the patient, you're describing, they have he's now diagnosis of heart failure which comes with a stigma and I think so she has heart failure with reduced ejection fraction, which is EF of 30% because anything less than 40% is reduced above 50 is preserved and between 40 to 50 is mid range. And then you have to go into those other criteria where somebody may be improved EF or totally recover ef. Well, we don't say recovery anymore. And I'm sure Michelle, Dr. Kittleson talked about this in our discussions with you as well. So that's number one. So heart failure with reduced ejection fraction. Then you also classify the stage of the cardiomyopathy. So Starting from early 2000s, aha, CC started classifying all these cardiomyopathies in stage A, B, C, D. And now we updated them a little bit more. We call it at risk of heart failure, stage B, stage C, stage D. So anybody who has symptoms by default is stage C. This is somebody, I would say stage C cardiomyopathy with heart failure with rejection fraction. Now, in her case, you know, just based on the presentations, she's also hypertensive and she has left ventricular hypertrophy. So there's likely etiology. Again, as your working diagnosis is she's likely hypertensive heart disease or hypertensive cardiomyopathy.

B (51:15)

And what about her, like mild to moderate mitral regurgitation? Anything to be thinking about, like finding the valvular abnormalities at this stage or would you kind of keep going down, just worrying about the heart failure, decongesting her and treating the heart failure and worrying about this new valvular insufficiency kind of from the outpatient side?

E (51:36)

Yeah, that was a great question because remember we talked referred to it a little bit earlier. So this is at time of diagnosis now. So you have early. This is early finding. You know, this is the time of new diagnosis. You are going to control the blood pressure, you're going to control the afterload, you're going to decongest it and then reassess it again. What is the degree of mitral regurgitation? You also, on the echocardiogram, you will want to know whether there's a prolapse of the mitral valve of those leaflets, if there's any structural or anatomical defect or is it just functional mitral regurgitation. So that would also you look at the echocardiogram, you look at the size of the ventricle. Is it very dilated? Is it like so much stretch on the mitral apparatus that on the ring that it's causing a functional mitral regurgitation? But anything you do is going to be first predicated on your initial treatment because you're not going to really treat the mitral regurgitation. Right now what you're treating is the cardiomyopathy. You're treating the heart failure, you're treating all the things assured with it. You're using your decongestion, getting them on the right therapies based on the phenotype now and then coming back later on and reassessing the mitral and then addressing if it's still persistent.

B (52:53)

Okay. And so knowing that she's ref, what drugs or therapies would you consider starting for her at this.

E (53:01)

So, you know, at this current time in 2024, I think you're in 24, right? Yeah, 24. We have quadruple Therapy, which is what we all say, the four pillars. And that should be your initial yet kind of platform, which is beta blockers, SGLT2 inhibitors, nepalycin inhibition with ARBs or angiotensin receptor blocker combination or as we commonly call it, arni. And the last one will be an aldosterone. So those will be the four basic pillars of treatment. Now, the sequence of it may vary a little bit depending on the situation, the kidney function, the blood pressure. But you know, as you alluded to earlier, SGLT2 early on now is kind of recommended even in, even in your consensus documents on acute heart failure, just because of the tolerability of it, as long as initially GFR is above 30. Now in chronic heart failure, the GFR criteria will change a little bit. But initially starting off therapy anywhere 20 to 30 and above is pretty reasonable. And then depending on the degree of pulmonary edema, depending on the renal function of blood pressure, you have Arnie's beta blockers and then you have the ultrasound antagonist. Now, what I would say say is the aldosterone antagonist, there's not real data on inpatient initiation and management on that, but what it is very well accepted because it has such a good or marginal effect on blood pressure, but helps with the kind of adjunct duresis on top of everything. And it's much more tolerated at the 25 milligram dose, at the beginning dose, especially as you're also dilucing people and they have, they tend to get hypokalemic. It helps with, you know, improving the potassium level. So it's a good kind of therapeutic target to address while they're in there. And then obviously there's now evidence to support that if you start it inpatient, obviously patients tend to stay on it outpatient as well.

B (55:17)

And then would you say beta blocker tends to be last given, like usually trying, like if you're decongesting and concerned for.

E (55:27)

So if you, if congestive heart failure is the initial thing. So that would be towards the last one before, prior to the charge. And then they're kind of euvolemic or, you know, and you are initiating the beta blocker. But a word of caution would be to say, you know, the patient should not be starting a beta blocker on the day of discharge on the way out of the hospital. You really want to see, give a little time period to see if they tolerate it well. And then, you know, at least a 24 hours in advance before the discharge.

B (55:58)

And then I guess in this era where I think like Arnia is becoming. I feel like the goal to start that those you would still try to start early if blood pressure could tolerate.

E (56:12)

Is that so you know, the way the trials were. So that's a good one because, you know, the way the trial. There are different trials. So there's kind of, you know, within acute heart failure also there are three different trials kind of looking at that. And in the pioneer HF there was which was kind of supportive for the role of Arnie's within the. In hospital stay. It was shown to be beneficial. And then later on there was a life study which was more focused on Class 4 heart failure patients. These were sicker patients. They were already had washouts. They had, you know, on enalapril and other agents. And then they were kind of included in the trial. And if you look at the degree of hypotension is much higher with Arnie's compared to ACE or arbs. So that's just the nature of the medication. Right. So that's why you have to just be careful on the blood pressure and the kidney function, the stability of it once they are in your. Because when you are actively diarrhusing them or, you know, decongesting them, there may be some fluctuations. So just be careful on starting that medication because then, you know, then the next thing happens. A lot of times in practice is people get so scared with the creatinine changing and they stop everything and then the diuretics get stopped too. So I. What I would say is if you still are very congested and and you're normal tensive, you first decongest the patient. Use your SGLT2. If you really need, you can use algastrone early on as well. And then as you are now shifting from, you know, whether continuous infusion to a bolus or bolus to oral strategy for diuretic, that's the time to start the arni.

B (57:56)

Okay, that's helpful.

C (57:58)

Yeah, I think actually they went through this similar thought process on the Dr. Kittleson episodes, especially about the renal function stuff. It's almost like I think. And they referred to Dr. Topp's episode about it, who's a nephrologist and talked about how like, you almost just don't want to check certain things and that's more outpatient, but very helpful to walk through. Again, how does this change if this is HFpEF, like the sequence of what I start what and do I start all of it? So, yeah, how does this change with HFpEF?

E (58:29)

So HFpEF, remember you went through with some of the kind of long term chronic management of HFEF with Michelle. Now there's some nuances in there based on gender and ejection fraction, male versus male, especially as it relates to Arnie's. But SGLT2 is across the board. All genders are EF. So I don't think there's much difference when it comes down to an acute heart failure whether you have HFP or HFrEF, you're using the diuretic and then you can straightaway go to SGLT2 alongside. So that would be the strategy. Now after that then the nuances come in depending on ARNI based on gender and injection fraction for women, across the whole range of injection fractions you can use an arnie for Men EF of less than 60% is where the biggest benefit has been for Arnie's Aldosterone antagonist clinically, even though the guidelines give it a 2A recommendation for more driven towards reducing rehospitalization. We know that evidence from some of the subgroups and also real life factors that they're very helpful to reduce rehospitalization and achieve more direct and especially if somebody's hypokalemic as well to improve the potassium levels too. So that really is useful there. And then beta blocker is very different compared to HFrEF. So the role of beta blocker is. There is no really a direct role of beta blocker in hfp unless there's another reason. So if somebody has arrhythmia, atrial fibrillation or ventricular arrhythmias or PVCs or they may have coronary artery disease, so there's another primary indication for a beta blocker that would be the. Then you would use that. But compared to HFrEF where it's across the board on everyone, this is a very specific population.

C (60:28)

Okay. And now that we have done all of that, I think the other question starts to become like trying to establish etiologies and obviously this patient has a lot of risk factors for coronary disease. I assume she needs an ischemic evaluation. I think the question I always have more than anything is is this something that I need to do before they go home or is this something that like let me get them decongested and started on these meds and then they can get that as an outpatient.

E (60:57)

So yeah, so that's the question about ischemic valuation. That's the one which comes up all the time. So first thing, it should be predicated to what are the Risk factors. So not everybody wants to or warrants ischemic valuation. So it should be driven out of what your risk is. Pre test probability. Now, if you have a 32 year old with no other risk and now you have hefrath, whether it's hypertensive or depending on where you practice, is it familial? Not everybody really needs to run into an ischemic evaluation and even the guidelines are pretty clear on that. But if you have risk factors or you have symptoms suggested of angina, that's the one where you really want to do inpatient evaluation. Also, sometimes from a kind of a logistical challenge perspective, it's easier to do it while they're in there to know the etiology of it. Now the question always is, what are you going to do with that information? Is there somebody, are you looking at a surgical revascularization, especially if they have no symptoms? Because that's where that topic comes up is if you find an etiology, if you have coronary stenosis, does it really explain the cardiomyopathy or the heart failure? And if that's the case, is that something treatable? So those are kind of different layers of questioning which come in. We routinely at Kashuk Memorial will do ischemic evaluation on patients who have risk factors. Especially they're, you know, also from a. Because they also serve a lot of underserved patients. So from a. From a totally logistics perspective, it's just easier for them to get it done while they're there. But it's okay that if their risk factors are not much and you know, you're not sure and there's a fluctuation going on in their renal function and you can then do it outpatient on a follow up.

C (62:58)

Okay. Yeah, I think we think about the resource stuff too for some of our patients too. So that's helpful to know.

B (63:04)

And the ischemic evaluation, does it have to be a cardiac catheterization?

E (63:09)

No. In today's day and age, not necessary at all. Again, you know, depending on your pretest probability and age and everything and what else is going on to somebody, you do not expect too advanced age or renal disease. So you don't think there's going to be too much calcification. You can do a CTA stress test is still there. You can still utilize the stress test. There's obviously as an advanced heart failure person, I can tell you that we see some patients who come later to us in their life journey for advanced therapies and they had stress test and then we end up doing a catheterization, and we find some significant disease. So because remember, the false negative rate can be there, especially if there's balance ischemia. So if you're really doing a true evaluation, it should be either a CTA or cardiac catheterization.

C (63:58)

Okay, great.

B (64:00)

So I think this is a great point for us to maybe just summarize. We've already talked about a lot, but before we kind of take the case down its next twisty turns, I just think that the few things that I wanted to highlight is just emphasizing when to get the echoes on which patient. So, obviously, new onset suspicion for heart failure to get your echo, but for everyone else to kind of make sure that you have a reason to be checking for it. And then I think the other thing to be thinking about is, you know, the patients that are coming in to be pretty lenient, I guess, and I don't know if that's exactly the right word, but starting the guideline directed, like medical therapies early, but being cognizant of their other comorbidities. And so it seems like kind of across the board, reasonable to start SGLT2s early. Often on these patients and everyone else, you're going to kind of have to be considerate of their other issues. Heart rates, blood pressures, all of those other things that we have to think about. And I don't know if there's anything else you wanted to add, Moni.

C (65:04)

No. SGLT2 is for everyone.

B (65:06)

I know. I think it was at SHM, we were like, oh, man, SGLT2 is having a party. And I just feel like we're reiterating that on this episode.

C (65:13)

The ride continues.

E (65:16)

Yeah. The SGLT2 is statin for heart failure.

B (65:19)

Yeah, I'm gonna be putting it in the water soon.

C (65:23)

That's a T shirt right there. All right, I'm gonna. I'll advance the case. So on hospital day three, Ms. Breath's condition worsens. Her blood pressure's now 95 over 60. Her heart rate's 125, and her oxygen saturation is 92% with 2 liters. And her urine output has significantly declined in the past 24 hours. And on exam, she's cool, and her legs are slightly modeled. So I think it's fair to say this is cardiogenic shock until proven otherwise. And so I think this is one of those things that we talk a lot about on these inpatient episodes where the diagnostics and the treatment are kind of having to happen in parallel. So anticipating that she'll be transferred to the ccu. I think we do kind of need to understand the next steps, but I think sometimes with logistical challenges, the transfer doesn't maybe happen as soon as this very scared, petrified hospitalist would like. And so sometimes I'm kind of told, you know, double the diuretic dose instead of the inotropes, which I can't start on the floor. So are there situations so that to me feels a little counterintuitive as somebody that doesn't work in the ccu. So are there situations which I can expect somebody who's like kind of already fallen off the wrong side of the Starling curve to actually respond in these situations to the doubling of the diuretics?

E (66:51)

So, you know, I think there's. It all will depend on what's going on. Right? There's a little more nuanced answer I'm going to give to this one. So is there a situation where somebody may get benefited from increased viruses is possible. It's possible in the sense that if they, it's not that they are dry, they're not dehydrated, they may still be volume overloaded, but they're in low output failure. So those are two things which go hand in hand. But their filling pressures are still high. They still may be in volume overload, but now they're also in low output failure. And that's why the blood pressure is low. And sometimes what happens is out of a worry that maybe, oh, maybe the diuretic is causing the low blood pressure. We start holding the diuretic in these patients when the answer is, you know, supportive therapy or blood pressure, where the inotropes, assessing hemodynamics and everything else. But I think before that, what you can do is while you are waiting for transport, I think this is something which is just kind of bedside things, making sure that they're still not getting some of the other neurohormonal agents which may have been started on. So making sure that we stop those, because that's kind of sometimes is because they are new therapies. They've been started on them and now they're hypotensive as well. But in this particular case, just based on the clinical definition of shock, 30 points lower than their average mean systolic of less than 90, obviously immortal skin, all the stuff suggestive of shock. So they really, really need. What they really need is kind of either a pulmonary artery catheter as well as inotropes or pressors, depending on what you're going to find on and that's also useful because that's also going to tell you what your volume status is, because a lot of these patients may still need an IV diuretic, but they just may need an inotrope or something else alongside for renal perfusion, too.

C (68:51)

Okay, and how do you think through which ones to start? I know I'm getting bold as a hospitalist here, but which ones to start and then is there any to avoid in this situation?

E (69:02)

Yeah, I mean, because here you are doing empiric. Right. Right now, because assuming that you don't have a swan, you don't have right heart cat on them. So you're doing empiric therapy assuming they are low output failure. So you want it depending on the blood pressure, if they are totally hypotensive. If they're like getting hypotensive, they have lactic acidosis from the hypotension. You really need to maintain their blood pressure and perfusion, which is across the board. As much as we hate that, you need a kind of V suppressor and that's going to be your first one just to maintain the blood pressure above a certain map. From an inotropy perspective, you can do. If you are hypotensive, you can use dopamine, but you have to be cognizant of the heart rate because if they tachycardia on top, that's going to make it worse. My choice usually is melurnon or dobutamine, depending on if I am suspecting that's low output failure in a cardiomyopathy patient. Those are the two ones I would usually go to. Melanin or dobutamine, again, depending on blood pressure. If they're already hypotensive, melanin is not going to be tolerated. Well, or if they are very tachycardic, you're not going to tolerate these either do but mean or dopamine or even melanin. Well, in that case, if you just may have to first bring up the pressure. And then obviously if they're really, really kind of fast arrhythmia or something going on, then you're talking about kind of more temporary mechanical devices and stuff, all that stuff. So that's the way I would see. Now there's the other caveat is in this particular patient, you're saying hypotensive. But if this could be somebody in shock and hypertensive goes back to Meredith, your vasodilator story. And that's where you would use things such as nitroglycerin and niprite. Again, not possible on the floor because no floor will allow you to start a nitroglycerinide across the. I don't think anywhere across the board, but that could be an option. If somebody was in shock, their lactic acid is going up, they're in pulmonary edema. And they still are if you really. And they still may hypertensive. And that's the case where you would use a pure, pure vessel dilator.

B (71:22)

Definitely thankful we don't work in an open icu, but there are certainly hospitals that hospitalists that do. So I think that's helpful to have that conversation. I think the other thing that goes with it is the diagnostic part of it. So like thinking about one who actually needs the right heart catheterization and then the timing of when that is actually the most helpful to you as like trying to figure out what's going on in the therapies they need to be on going forward.

E (71:49)

Yeah, so this comes up across a lot now, you know, assuming we're still talking about this particular patient, but I'll first start with that and I'll go to a general kind of criteria. In this particular patient, she's already declared herself. Right. So you really need to know, and this is a patient you're upgrading to the CCU or the CICU or icu, whatever that infrastructure is in your hospital. So now that's a patient who needs a swan right there. You know, assessment of their filling pressures, assessment of their cardiac output, all the stuff that's number one. Now this is obviously more of you in the shocky state, but there are a lot of other patients who may not be in that state. Those are the ones who, you know, may be either getting hypotensive, they may not be shocky, but they are getting hypotensive. Or you have to peel back on therapy. They came on therapy. This is acute on chronic heart failure. They're already on good medications to begin with. You're just diagnosing them, doing all the things, and now suddenly you're peeling off medication. So this is where you should really think about, okay, why am I have to cut back on medication or stop medication or they're not responding to your dietic strategy or their kidney function is getting worse. So those are kind of three or their symptoms are not improving. I mean, those are four kind of big classes or situations where you would want a right fit cat.

B (73:09)

Okay, so let's go back to Ms. Breath. She briefly requires to stay in the CCU. She gets her inotropic support and she's actually able to wean off of it. After she's dry she gets transferred back to the floor and now she's on room air. Edema's improved everything and so now we're trying to think getting her ready for discharge a little bit. So what medications, let's start with that first are we focusing on at this point?

E (73:42)

So you know, assuming this was all cardiogenic shock from low output failure and you know, somehow she was in that still state where she didn't need more advanced therapies and she's off the curve, she is back in the lower quadrant on your hemodynamic profile and now you're going to start medication. So again the most tolerable medication would be an SGLC2 inhibitor and then depending on your blood pressure you could do Aldrich antagonist. If your blood pressure is reasonable you can add an Arnie. I would be a little cautious on introduction of beta blocker at this point. If they were truly in shock, they were in icu on inotropes introduction of beta blocker I would delay it at this point. This is in fact it again all depends on, you know, how many days you're going to be in there, what else is going on. But you know, if this is very close to her discharge state, to whether hospital, whether home or anywhere else, then I would actually even defer the beta blocking introduction to the first follow up visit. Now if she's still there and she has a robust blood pressure and you know, despite introduction of the other three classes of medication, then you could do an introduction of beta blocker as the last one Again.

B (75:00)

So this is like my age old question and I feel like this is why we're doing this episode. What should I favor? Is it better for someone to be on the lowest doses of all four pillars of medication or to be starting to titrate them higher on the medications that they can tolerate?

E (75:20)

Yeah, no, this is an absolutely super important question and is being kind of, it's being addressed everywhere, you know, again in documents, on the podiums, on everywhere. Because more and more evidence is that low dose of all is much superior than higher dose of a few. Because you think about it, you're addressing different pathways so you're getting incremental benefit, additive benefit of different pathways of blockage or you know, modulation and that's what you will miss. And also patients tend to tolerate more the lower doses and higher doses of one. So more the merrier would be the principle. And so you would start off all the lowest doses of four. Then if they're able to tolerate, then you would escalate them.

B (76:11)

All right, well, that answer that.

C (76:13)

Yeah, that's definitely the one. I think the reason that Meredith said this is like the whole reason we're having the episode is, as I've referred to in the past, I'm just a petrified hospitalist at baseline when it comes to this stuff. And so sometimes I kind of feel like I've seen some of my patients get readmitted with pre syncope and I sent them out on all these medications and it's probably just. Probably as not happen very often, but that's the one. Those are the ones you remember, right? And so I don't know, do you have any words to sort of like make me feel better about this?

E (76:50)

Yeah. No. So I think that's an important question because I think it happens. It will happen. And I think that's where nuances will come in. Nuances like you gotta look at the patient age, you know, what else is going on? Is there something which is causing the autonomic dysfunction? Are they dehydrated? So what happens is it goes back to what we had initially talked about. You know, you started SGLT2 in the past. We didn't have that. Now you have HGLT2 and can give a pretty potent diuresis. You started the Albus antagonist in the past. You know, if you look at the Medicare data, anywhere between 30 to 60% of the patients are on an MRA. And so now if you are pushing it, which is the right thing to do, that's going to help you with diuretic too. So this is where you need to adjust that dose of your regular loop diuretic before they go out. And that's kind of the important thing. So you, yes, you got all the four medications. And because Arnie's are going to help also with the afterload reduction accentuated diuresis. So as you are getting those three classes of medications on you, just make sure that the patient is kind of not totally dehydrated. And the same thing as I said about beta blocker that don't do it the day of discharge because you want to see if they were able to tolerate it for a day. And unfortunately, in the current world, in the United States, we have one of the shortest hospital stay durations around the world for heart failure. The duration of heart failure stay is one of the shortest around the world in. In the United States. So what happens is we are packing up so Much within that duration. Because we also know when patients go out without those four medications, a lot of them will never end up going on that I'm sure you discussed the evolution HF and other. There's a large registry showing patients who were started on medications, the four classes. And by the end of one year, a majority of them were either not on medication or where there was a reduction in dose. Two thirds of the patients, you know, were off beta blocker doses and MRAs and everything at the end of one year. So this is a real problem. So yes, there's a rare chance of somebody coming back with presyncope. It's usually because we didn't address the diuretic dose before they went out and we, you know, maybe we adjusted the dose the day off and they went out and now they're back game.

B (79:21)

I think that probably is what happens because I feel like even during my relatively short career so far, I think the guidelines had changed during them. And so that's when it like became recommended, I believe, to watch someone when you start their oral diuretic before they go. But I definitely don't think about it as much for like the other guideline therapies. And I think because of the recent studies kind of recommending, you know, relatively quick titration in the hospital, it definitely sometimes feels like I'm throwing it to them as they're walking out the door and then praying that nothing bad happens.

E (79:59)

So this is where, you know, there's other things, things you can do is obviously, you know, you have to be careful with the age like octogenarians and, and you have to be careful because, you know, sometimes that may be a population where you may have to be gentle as much as I like to be aggressive, but they may or may not tolerate those. So, you know, one size doesn't always fit all even though we, we want that thing to happen. Other thing you can do is the, you know, you can always do orthostatic vitals on these patients, especially the elderly patients, before discharge will kind of get you an idea other than just clinical exam, which we don't utilize orthostatic vitals as much because usually that's what kind of makes them fall and is that orthostasis. So that will also get you a little bit more comfortable whether they are. What's the volume status in there?

B (80:50)

Yeah, I like that.

E (80:52)

And then the other thing is like, you know, as you transition, which is the, the other bigger picture is the, is the, the post discharge follow up because you really need that that's kind of how soon can they be seen and reassessed?

B (81:07)

Yeah, I mean, I think that's the other part that often comes up is, you know, the trials all had very quick follow ups, like within a few days. And I just don't think that that's realistic. And so I think that's the other part that's a struggle when I like part of why I don't want to add everything when they're going. Cause I don't actually know when they're going to be seen.

E (81:27)

So, you know, at Kashluq Memorial we actually do. And I think a lot of the centers who are now focused on quality of care around readmissions and everything, investing in those systems. We actually have our patients seen in our discharge clinics by our care providers and extenders and apps within a week of discharge. So they are, unless there is somebody who doesn't come for totally different reason, but they all get an appointment within a week to look at the volume status, adjusting the dose of diuretics, the medication dose with the base on blood pressure, getting their blood work done, making sure they're no renal injury or hypokalemia or anything like that.

C (82:13)

I think one of the things that was, that caught me off guard early when we were kind of implementing all these new guideline directed therapies was this washout period for, you know, ACE and ARB stuff. So I was curious your thoughts on the need for that versus not because certainly that adds to length of stay, which, you know, whether or not that's an important metric, we can, that's for another episode, but specifically about the washout period.

E (82:38)

So the washout period is very important. I don't think there's any, any question about that, especially coming off an ACE into an Arnie because there's an actual risk of, you know, injuredema. And so I don't think, you know, and that's why it's very clear on the labeling as well. One of the few things which is very clear. So you really want the 36 hour washout period now. I mean, if this is a length of stay issue, I'm sure as you said, you can talk at another time, but that's a different story. You can always do an arb. You can start an ARB and that can be replaced pretty easily or you can start an ARB and then they can go out and get into an arnie.

C (83:18)

Okay. And I think one of the things that was they actually cover this at length in the outpatient episodes. But just as have said it here, the cost of the Arni has become kind of prohibitive for a lot of patients, I think. And so just kind of keeping that in mind is important. Obviously we have other options that aren't as good, but obviously it's better than not having anything at all.

E (83:40)

Yeah. So, you know, and that's actually what the, even the guideline writers acknowledge that, that you know, because of different either whether side effects or cost could be a factor in some patients. If that's withstanding those two factors, everybody should preferably an RNA as Class 1. But if that's a factor. Now remember, a lot of the patients on federal insurances cannot get other assistance at the current time. The out of pocket expenses are getting limited now. And by next year, based on the current negotiations between the cost of medication as well as out of pocket expenses for seniors, that's going to be limited to a certain amount which is going to be for all medications. So that's going to be really cutting down that out of pocket cost for patients after that. So that's definitely there. But that is still a problem, which can be for some people that much amount as well in that case, making sure they are on ARB instead. But they are assistance programs, I think, and this is kind of key is, you know, working with the case managers that the court transition coordinators or outpatient clinics to make sure you can tap into those assistance programs. Because there's a whether from the vendor itself, whether from, you know, if somebody cannot really afford to cover the cost of it, we actually, we try to get them all those other assistance.

C (85:07)

Great. And we've talked a little bit about appointment timing within the first two weeks after discharge. I think the other part that I try to stress with my teams is sort of the patient education piece, especially in someone like this patient who's a new diagnosis, who's sort of managing their diuretics and things like that. So could you maybe walk us through how you like to think through that and explain that to patients?

E (85:31)

Yeah. So, you know, patient education is so important. And this should start right. The journey should start right in the hospital itself because you have a captive audience at that time. Now remember, a lot of the retention, the rate of retention is going to be low because there's so much going on that time. So it's not just once and done kind of deal. This is an ongoing journey and ongoing effort. And this is where that team effort comes in between inpatient outpatient teams. And if obviously they're spread around inpatient, you know, starting from you know, the medical teams walking through the diagnosis, explaining them what that means, what that kind of the medications mean, what each medication's perceived side effect could be, because that's where a lot of the discontinuation is, because the patients were not aware of the perceived side effect. So and when that side effect happens, what happens is they stop it because they were not aware about it. But what I find very commonly is when you talk through and you explain the patient what that side effect is and when they feel it, if it's not something which is major, they say, okay, I know about it. This was expected. Even things like orthostatic dizziness sometimes, and especially neurohormonal blockers, if they're aware that panic level goes away, then talking about the disease state, things such as diet, lifestyle, exercise, you know, sodium fluid, all those things. Awareness of how to be, you know, aware about when they're decompensating again, or you know, what to do, what to, how to titrate some of the medications, diuretics, if they're reliable on their own, and then the diagnosis per se, what that diagnosis really means and what that kind of prognosis. Now I do tend not to talk about numbers right up front about mortality and this and that because that does make people very upset and panicky because already hearing heart failure is a kind of a, you know, a scary thing to kind of start with. But then also utilizing your pharmacist, depending on again, each system, there may be pharmacists, there may be care coordinators, there may be, you know, social workers, bedside nursing, all of them. So having different layers of education is important because one person just, you know, the cardiologist, the hospitalist is not enough because that just, you know, you're going in, you're talking, it needs recurrent reinforcement of the diagnosis, the change in lifestyle, all those kind of things. Every time they get a medication administration, they need to talk. And then that journey continues as they come to a follow up appointment. Obviously, depending on the system, there'll be things such as community navigators. We have community health workers which go to the house right after discharge, look at the kind of home environment, help them at home again, educating them about the diagnosis, what they need to do, keeping the appointments, all the stuff. And then on the outpatient ambulatory follow up, that journey of education should continue.

B (88:39)

Awesome. I think that's a good place where we could do take home points. So what are like maybe your three take home points for the listeners from, you know, what you want to make sure. They take away from this episode.

E (88:51)

Yeah. I think one other thing is, you know, I would say decongestive therapy. You know, you gotta be, you gotta go aggressive. If you know somebody's overloaded, just don't, you know, I say don't massage the same thing till death. You know, escalate therapy quickly. If non responsive, go to the next level either if bolus, then increase the frequency if continuous but do something different. Number one, institute some of those medication classes we talked about early on, especially at GLT2 as we talked about they are, you know, you can really strategize based on blood pressure, you know, whether MRAs, it's more like one or none kind of phenomena. There's a gray area in there. So if you cannot tolerate Arnie's or beta blockers, you still can do SGLT2 and MRI. The last thing I would say is education is key and making sure that transition of care is important because that's the key focus in overall outcome. That's what's going to decide what's going to happen in 30 days, 90 days and long term, that transitional period, making sure patients have the right medications. The doses are if somebody was already on before and now they really know what they're going home on. They really have those, if there's a possibility, have those medicines at bedside. If they don't have it, making sure when the pharmacy you're sending it, they have those medications. A lot of times we send patients home and they get, we send them to the pharmacy. Lot of pharmacies may not even have the medication or they need a prioritization. And so patient shows up after discharge and there's no medications now and then we know what that results in. So that's kind of what I would say.

B (90:33)

Awesome. This has been another episode of the Curbsiders bringing you a little knowledge food for your brain hole.

C (90:43)

Yummy.

B (90:44)

Still hungry for more.

E (90:45)

More.

C (90:45)

Yep.

B (90:46)

Join our Patreon and get all episodes ad free twice monthly bonus episodes. At patreon.com curbsiders you can find shownothecurbsiders.com and sign up for our mailing list to get our weekly show notes in your inbox including our Curbsiders digest recapping the latest practice, changing articles, guidelines and news in internal medicine.

C (91:05)

And here at the Curbsiders we're committed to high value practice changing knowledge. And to do that we need your feedback. So please email us@askcurbsidersmail.com it also helps a ton when you subscribe, rate and review the show on YouTube, Spotify or Apple Podcasts.

B (91:19)

A special thanks to our writer producers for the episode RJ Blackburn and to our whole Curbsiders team. Our technical production is done by the team at podpace. Elizabeth Proto does our social media. Jen Watto runs our Patreon. Chris the Chew Manchu moderates our Discord. Stuart composed the theme music and with all of that, until next time, I've.

C (91:40)

Been Meredith Trubitt and as always, I've been Moni Amin. Thank you and good night.

E (92:02)

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